Obstetrics - Abnormal pregnancy Flashcards
One of the strongest risk factors for ectopic pregnancy is
prior ectopic pregnancy
- On laboratory studies, the classic finding is a β-hCG level that is low for gestational age and does not increase at the expected rate
Patients who present with an unruptured ectopic pregnancy can be treated
surgically or medically.
MTX for medical, uncomplicated, nonthreatening ectopics
1st trimester spontaneous abortion
most are 2/2 abnormal chromosomes, of which 95% are due to errors in maternal gametogenesis.
A patient with a threatened abortion should be followed for continued bleeding and placed on pelvic rest with nothing per vagina. Often, the bleeding will resolve. However, these patients are at increased risk for preterm labor (PTL) and preterm premature rupture of membranes (PPROM).
All Rh-negative pregnant women who experience
vaginal bleeding during pregnancy should receive RhoGAM to prevent isoimmunization
2nd trimester spontaneous abortion
Infection, maternal uterine or cervical anatomic defects, maternal systemic disease, exposure to fetotoxic agents, and trauma are all associated with late abortions.
Cervical incompetence is estimated to cause approximately 15% of all second-trimester losses
- place cerclage at 12 wks —> 38 weeks take out
Recurrent pregnancy loss - what do you think of?
chromosomal abnormalities,
maternal systemic disease,
maternal anatomic defects,
infection.
Workup:
- antiphospholipid antibody (APA) syndrome.
- luteal phase defect —> lack an adequate level
of progesterone to maintain the pregnancy
Genetics question - 2 aa spouses, no SCD. Husband’s brother has sickle cell. Carrier rate in aa is 1/10.
What are chance baby has SCD?
Sickle cell anemia is an autosomal recessive condition that occurs in 1/500 births in the African-American population. The carrier state, or sickle-cell trait, is found in approximately 1/10 African-Americans. Since the patient’s brother is affected, both of their parents have to be carriers. Each time two carrier parents for an autosomal recessive condition conceive there is a 1/4 chance of having either an affected or an unaffected child and a 1/2 chance of having a child who is a carrier. Since the patient is unaffected, she has a 1/3 chance of not being a carrier and a 2/3 chance of being a carrier. The patient’s husband has a 1/10 chance of being a carrier (the general population risk for African-Americans). Thus, the chance that this couple will have a child with sickle cell anemia is: 2/3 X 1/10 X 1/4 = 1/60.
A spontaneous abortion (SAB), or miscarriage, is
a pregnancy that ends before 20 weeks’ gestation.
Complete abortion
complete expulsion of all POC before 20 weeks’
gestation
Cervix closes after expulsion
Associated pain and uterine contractions stop
US = empty uterus
Incomplete abortion
- what is it
- clinical sx
- cervix
- US
- tx
partial expulsion of some but not all POC before 20 weeks’ gestation.
Clinical sx
- vaginal bleeding w/ passage of large clots or tissue
- uterine cramps
- products of conception often visualized in dilated cervical os
Os - OPEN
US = some fetal tissue, products of conception often in cervix
Tx
- D&C or expectant management or med management (prostaglandins)
Inevitable abortion
- what is it
- clinical sx
- cervix
- US
- tx
+/- expulsion of products, but vaginal bleeding and dilation of the cervix such that a viable pregnancy is unlikely.
Clinical sx
- vaginal bleeding
- uterine cramps
- possible intrauterine fetus w/ heartbeat
- May be able to see products of conception through dilated cervix
Os - OPEN
US = ruptured or collapsed gestational sac +/- fetal heartbeat
***Same presentation as missed ab but it is INCOMPLETE (vs no) evacuation of conceptus and will have lower abdominal cramps
Tx
- D&C or expectant mangement or med management (prostaglandins)
Threatened abortion
- what is it
- clinical sx
- cervix
- us
- Tx
Vaginal bleeding before 20 weeks without the passage of any products.
Clinical sx
- variable amt vaginal bleeding
- pregnancy can go to viable birth
OS - CLOSED
US - Fetus alive, + FHR
Tx - reassure and outpatient followup
Missed abortion
- what is it
- clinical sx
- cervix
- US
- Tx
death of the embryo or fetus before 20 weeks with
complete retention of all POC
Clinical signs
- no sx - light vaginal bleeding
- pregnancy sx may decrease
- Suspect when STOP N/V of early pregnancy and arrest of uterine growth
Os - CLOSED
US - ruptured or collapsed gestational sac with no fetal cardiac activity
Tx
- D&C, expectant manage, med manage (prostaglandins)
IUGR in gest diabetes vs prediabetes?
What things are seen in each?
IUGR in pregestational DM, not GDM
Small babies –> type 1 or pregestational
Macrosomiic babies –> GDM
- Risks: Shoulder dystocia, metabolic disturbances, preeclampsia, polyhydramnios and fetal macrosomia are all associated risks of gestational diabetes
Major causes of antepartum hemorrhage
Placenta previa**
Plactental abruption**
Uterine rupture
Fetal vessel rupture
Placenta previa
abnormal implantation over internal cervical os
Can be complicated by placenta accreta
accounts for 20% antepartum hemorrhage
Happens in 0.5% preggers
Need to do c/s
- if term, do scheduled
- if 36 weeks –> amnio to assess lung maturity
Vasa previa
Velamentous cord insertion causes fetal vessels to pass over internal cervical os
fetal blood vessels cross fetal membranes in lower segment of uterus between fetus adn internal cervical os
Painless antepartum hemorrhage
rapid deterioration of fetal heart tracing as hemorrhage is fetal origin
Succenturiate lobe
If placenta grows over cervix, which is less well vascularized, can atrophy incompletely causing a placental lobe discrete from teh rest of the placenta
Bleeding from a placenta previa results from
small disruptions in the placental attachment during normal development and thinning of the lower uterine segment during the third trimester
This bleeding may stimulate further uterine contractions,
which in turn stimulates further placental separation and
bleeding.
Placenta accreta
Superficial attachment of placenta uterine myometrium
Placenta can’t separate from uterine wall after delivery of fetus –> hemorrhage and shock
Placenta increta
plcenta invades myometrium
Placenta percreta
Placenta invades through myometrium to uterine serosa
May invade other organs
Increased risk for placenta previa in
Prior uterine surgery (myometcomy, c/s)
Uterine anomalies
Multiple gestations
Multiparity
Advanced maternal age
Smoking
Prev placenta previa
Presentation of placenta previa
Painless vaginal bleeding
DO NOT DO A VAGINAL EXAM! May injure placenta –> hemorrhage
Velamentous placenta
Blood vessels insert between amnion and chorion, away from margin of placenta, leaving vessels largely unprotected and vulnerable to compression or injury
How should you dx placenta previa?
With transvaginal US
- is safe!
Placenta abruption
Premature separation of normally implanted placenta from uterine wall –> hemorrhage between uterine wall and placenta
Predisposing and precipitating factors for placental abruption
predisposing
- HTN
- prev placental abruption
- advanted maternal age
- polyhydramnios
- DM
- vascular insufficiency
- cocaine, meth, cigs, etoh
Precipitating
- trauma
- ROM with polyhydramnios
- PPROM
Presentation of placental abruption
3rd trimester vaginal bleeding
- severe abdominal pain
- strong ctx
Firm, tender uterus
Couvelaire uterus
- only seen at time of c/s
- blood from abruption infiltrates myometrium –> seorsa and gives bluish purple tone that can be seen on surface of uterus
Can try to dx previa vs abruption via US (always do) but not seeing one does not rule it out
Hypovolemic shock
Consumptive coagulopathy
Risk factors for uterine rupture
prior uterine surgery/scar
Lots of oxytocin
Multiparity
Uterine distention
Large fetus
Trauma
S/p repair of uterine rupture - what do you do for future pregnancies?
Try to tell them not to get pregnant!
If they do, repeat c/s at 36 weeks after confirm fetal lung matruity or at 37 weeks without testing for fetal lung matuirty
Fetal vessel rupture
Mostly 2/2 velamentous cord insertion
Can cause vasa previa or succenturiate lobes
Dx with US
Present w/ vaginal bleeding + sinusoidal FHR pattern –> immediate c/s!
Apt test
Can be used during time of vaginal bleeding
Examine blood for nucleated (fetal) RBCs
If mix is pink = fetal blood
Yellow brown = maternal blood
Sinusoidal pattern on FHR monitoring =
fetal anemia
Variable decelerations
Cord compression/prolapse
Oligohydramnios
Late decelerations
Uteroplatental insufficiency
SGA can be divided in
Decreased growth potential
IUGR
Decreased growth potential reasons
Congenital abnormalities
Teratogens
- EtOH
- cigs
Infxn
- CMV
- rubella
Anytime a fundal height is ____ less than expected, fetal growth should be estimated via ________
3 cm
ultrasound
Suspect IUGR
Normal flow through the umbilical artery is higher during
systole
The flow during diastole should never be absent
However, in the setting of increased placental resistance, which can be seen with a thrombosed or calcifed placenta, diastolic fl ow decreases or even becomes
absent or reversed. Reversed diastolic flow is particularly
concerning and is associated with a high risk of intrauterine fetal demise.
Macrosomia vs LGA
LGA = EFW > 90th percentile
Macrosomia = BW > 4500 in non-diabetic or BW > 4000 in diabetic
Risk factors for macrosomia
Diabetes Obesity Postterm preggers Previous LGA or macrosomia Maternal stature Multiparity Male infant Beckwith-Wiedemann syndrome
oligohydramnios
- def
- causes
1 cause of oligohydramnios = ROM
AFI < 5 by S
Decreased production or increased withdrawl
Chronic uteroplacental insufficiency (fetus doesn’t have nutrients or blood volume to maintain adequate GFR)
GU anomalies (potter syndrome, PCKD, obstruction)
Tx oligohydramnios
Depends on underlying etiology
Labor if
- term
- ROM
If GU anomalies
- MFM consult
Amnioinfusion
Polyhydramnios
- def
- causes
AFI > 20 or 25
NOT good!
Diabetes
Hydrops 2/2 high output cardiac failure
Multiple gestation
TE fistula, duodenal atresia
Erythroblastosis fetalis
In sensitized Rh- mother who has a Rh+ baby
Hyperdynamic state Heart failure Diffuse edema Ascites Pericardial effusion
How to tx unsensitized Rh- mom?
RhoGAM should be administered at 28 weeks and postpartum if the neonate is Rh positive
Tx sensitized Rh - mom
Follow antibody titers q 4 weeks
If baby Rh +, screen fetal anemia with MCA doppler measurements (increased peak systolic velocity measurements = concern for anemia)
Can also use serial amniocentesis, but usually use MCA doppler. Use amniocentesis if questionable results
Retained intrauterine fetal demise (IUFD) > 3-4 weeks can lead to
Hypofibrinogenemia —> DIC!
Make sure you evacuate the baby or deliver!
Postterm pregnancy
> 42 wks GA
or
> 294 days past LMP
Twin twin transfusion syndrome
2/2 unequal flow within vascular communications between twins in their shared placenta!
One twin will become donor, the other recipient
- donor will become anemic, IUGR, oligohydramnios
- recipient will be polyhydramnios, and may lead to heart failure and hydrops
Risk in Mono-Di twins
Examine US q 2 weeks to make sure amniotic fluid is equal
Tx
- serial amnio reduction
- coagulating vessels causing TTS
Risks with Mo-mo twins
Cord entaglement
Intrauterine fetal death
Usually deliver with c/s
Dx appendicitis in pregnancy
clinical findings and graded compression ultrasonography that is sensitive and specific especially before 35 weeks gestation
Macrosomic neonates are most at risk for
neonatal jaundice, hypoglycemia, birth trauma, hypocalcemia, childhood cancers such as leukemia, osteosarcoma, or Wilms tumor
When do you perform NSTs?
NSTs are generally not indicated in a routine pregnancy
until the pregnancy goes into the 41st week
Use in high risk starting at 32-34 weeks GA or when decrease in fetal mvmts in any pregnancy
Reactive
- 2 fetal HR accels / 20 mins
- repeat weekly
Nonreactive
- most common reason is sleeping baby –> use vibroacoustic stimulation to wake up baby
If still not reactive with vibroacoustic stim –> BPP use
Preeclampsia - pathogenesis
Dx by presence of
- nondependent edema (no longer components of dx)
- HTN
- Proteinuria
Pathophys
- generalized arteriolar constriction (vasospasm)
- intravascular depeltion 2/2 generalized transudative edema
- produces sx related to ischemia, necrosis, hemorrage of organs
HELLP syndrome
Subcategory of preeclampsia
Hemolysis
- schistocytes
- LDH elevation
- elevated bilirubin
Elevated LFTs
Low Platelets
Very serious!
More likely to be < 36 wks gestation
Warning signs: RUQ pain Epigastric pain N/V esp in 3rd trimester!
If see HTN early in second trimester, what do you consider?
Hydatidiform mole
Prev undiagnosed chronic HTN
Risk factors for preeclampsia
Chronic HTN Chronic renal dz Collagen vascular disease African american Maternal age (v young or v old)
Nulliparity
Prev preeclampsia
Multiple gestation
Abnormal placentation
Mother in law
Cohabitation < 1 y
Fetal complications of preeclampsia
Acute Uteroplacental insufficiency
- placental infarct and/or abruption
- intrapartum fetal distress
- still birth
Chronic uteroplacental insufficiency
- SGA fetuses
- IUGR
Oligohydramnios
Increased premmies
Increased c/s
Maternal complications of preeclampsia
Seizure Cerebral hemorrhage DIC Renal failure Hepatic failure
Pulm edema**
- endothelial damage –> increased vascular permeability
- decreased albumin
- decreased renal function
- arterial vasospasm –> increased vascular R –> decreased CO with CHF
Crtieria to dx Gestational HTN
SBP > 140 or DBP > 90
- should have BP elevated at least 2x 4-6 hrs apart, taken while seated
Criteria to dx mild preeclampsia
SBP > 140 or DBP > 90
- 2x taken 4-6 hrs apart
Proteinuria
> 300 mg/24h
or
1-2+ on dipstick
Criteria to dx severe preeclampsia
SBP > 160 or DBP > 110
OR signs/sx of severe preeclampsia
HA Visual changes, scotoma Pulm edema Acute renal failure Oliguria Proteinuria RUQ pain LFT elevation Hemolytic anemia Thrombocytopenia DIC IUGR, abnl umbilical dopplers
Criteria to dx Eclapmsia
Seizure! - grandmal
Complications:
- cerebral hemorrhage
- aspiration pna
- hypoxic encephalopathy
- thromboembolic events
Acute fatty liver of pregnancy
vs HELLP, lab tests below are associated wtih AFLP:
- elevated NH4
- blood glucose < 50
- reduced fibrinogen adn antithrombin III
Tx mild preeclampsia
Induction of labor:
- term
- unstable preterm
- fetal lung maturity present
C/s for ob indication
IV hydralazine or labetalol for BP
Betamethasone for fetal lung matuity
MgSO4 for seizure ppx
Tx severe preeclampsia
Goals
- prevent eclampsia
- control maternal BP
- deliver fetus
+ MgSO4, hydralazine or labetalol
Betamethasone if 24-32 weeks
> 32 weeks, deliver immediately!
Continue seizure ppx 24 hrs postpartum
Contraindications to expectant management:
- thrombocytopenia < 100,000
- inability to control blood pressure with maximum doses of 2 antihypertensive medications,
- non-reassuring fetal surveillance,
- liver function test > 2x normal,
- eclampsia,
- persistent CNS (central nervous system) symptoms
- oliguria.
Delivery should not be based on the degree of proteinuria.
Tx ecclampsia
Seizure management
- MgSO4
BP control
- hydralazine
Ppx for convulsions
- MgSO4 (continue until 12-24 hrs after delivery)
Deliver baby when mother stabilized
What do you do if MgSO4 OD?
CaCl or Ca gluconate for cardiac protection
Therapeutic: 4-7 mEq/L
Lose DTR: 7-10
Resp depression: 11
Cardiac arrest: 15
Pulmonary edema can occur with magnesium therapy, but is not related to toxicity from the drug.
Most common anti-HTN used in preggers?
Labetalol
NIfedipine
Superimposed preeclampsia on chronic HTN….how to dx?
increase in SBP of 30
When do most eclamptic seizures happen?
during labor
How do you get increased insulin resistance and generalized carb intolerance in preggers?
Human placental lactogen (and others) act as anti insulin agents
Gestational vs pregestational diabetes risks on fetus
GDM not at risk for congenital anomalies as much as pregestational diabetes
Macrosomia in GDM vs. IUGR in pregestational diabetes 2/2 uteroplacental insufficiency
But both have risk of
macrosomia
birth injuries
neonatal hypoglycemia, hypocalcemia, hyperbilirubinemia, polycythemia
As a result of the increased glucose load, the fetus secretes more insulin. As a growth factor, increased insulin levels result in increased fetal growth. I
This central deposition of fat is characteristic of diabetic macrosomia and underlies the dangers associated with vaginal delivery in these pregnancies.
